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M Selmanoff

Publications and source records attributed to M Selmanoff.

42 records · Page 3Linked to original sources
PubMed1984

Autofeedback effects of prolactin on basal, suckling-induced, and proestrous secretion of prolactin.

Subcutaneous injections of ovine prolactin (oPRL, 4 mg/kg) were utilized to study the negative feedback effect of PRL on its own secretion in lactating and 4-day estrous cycling female rats. Basal PRL secretion in the 10-day postpartum lactating rat is not suppressed by acute or 48 hr of exposure to oPRL. In contrast, basal PRL secretion on the morning of proestrus is inhibited following 48 hr of exposure to oPRL. Thus, the lactating rat appears to be unresponsive to the negative feedback action of PRL compared with the adult female rat in regards to basal PRL secretion. The suckling-induced PRL response is partially suppressed by exposure to oPRL in 10-day postpartum lactating rats. Considering the areas under the PRL response curves, the suckling-induced release is blunted by 6 (decreased 49%), 12 (decreased 46%), and 48 (decreased 77%) hr of oPRL exposure compared to controls. In contrast, in cycling animals, 48 hr of exposure to elevated oPRL levels dramatically abolished the proestrous PRL surge. Elevated PRL levels, by a direct action on the brain and/or indirectly by altering ovarian function, inhibit or override the hypothalamic mechanism(s) mediating the proestrous PRL surge while having a lesser effect on the mechanism(s) mediating the suckling-induced PRL response. Taken together, the present data point to probable differences in the mechanism(s) mediating basal, suckling-induced, and the proestrous secretion of prolactin.

Animals↗
PubMed1983

Role of pup age, estradiol-17 beta and pituitary responsiveness in the differences in the suckling-induced prolactin response during early and late lactation.

The suckling-induced prolactin (Prl) response was studied in 10- and 20-day postpartum female rats. The response in 20-day postpartum mothers has a slower onset, has markedly reduced peak values and returns to baseline somewhat sooner than the response in 10-day postpartum mothers. The blunted response of late lactation was seen in mothers suckled for 30 min and was maintained over a longer interval in mothers continuously suckled for 120 min. This refractory phenomenon was not due to decreased suckling intensity provided by 20-day relative to 10-day-old pups. Pituitary gland Prl release in response to thyrotropin releasing hormone (TRH) and haloperidol challenges also did not distinguish 10- from 20-day postpartum mothers. Significantly higher estradiol-17 beta levels were found in 20-day compared with 10-day postpartum mothers, a finding which cannot account for the blunted response. Pup separation from 10-day postpartum mothers for 4, 24, 48 or 72 h did not produce a blunted response like that seen in late lactation. It is suggested that the hypothalamic mechanism mediating suckling-induced Prl release becomes refractory to the suckling stimulus during the preweaning period.

Animals↗
PubMed1981

Decreased dopamine turnover in the median eminence in response to suckling in the lactating rat.

The effects of suckling on the turnover of dopamine (DA) and norepinephrine (NE) were studied in terminal projection fields of the tuberoinfundibular (median eminence, ME), nigrostriatal (caudate nucleus, CN), incertohypothalamic (medial preoptic nucleus, MPN) and mesolimbic (nucleus accumbens, NA) dopaminergic neurons. Decreased dopamine turnover in the median eminence was found in suckled compared with nonsuckled rats at 10 days postpartum. This effect was specific as dopamine turnover in the CN, NA and MPN and norepinephrine turnover in the ME, NA and MPN were not affected by suckling. The suckling-induced prolactin response is markedly blunted in rats 20 days postpartum. In these rats, median eminence dopamine turnover did not decrease significantly in response to suckling. These results are consistent with the hypothesis that median eminence dopamine is a physiological prolactin inhibitory factor mediating suckling-induced prolactin release.

Animals↗
PubMed1981

The lateral and medial median eminence: distribution of dopamine, norepinephrine, and luteinizing hormone-releasing hormone and the effect of prolactin on catecholamine turnover.

In the adult male rat, we have succeeded in microdissecting the median eminence into a LHRH-rich lateral region (MEl) and a LHRH-poor medial region (MEm). Dissected in this manner, the MEm has a 4.8-fold lower LHRH concentration and a 1.5-fold higher DA concentration than the MEl. The concentration of norepinephrine (NE) is not different in the two regions. Estimates of the rate constants for dopamine (DA) and NE decay after synthesis inhibition revealed no significant differences between the MEl and MEm kinetics for either amine. Hyperprolactinemia, produced by ovine PRL administration, resulted in marked increases in DA turnover rates in both the MEm (2.7-fold) and the MEl (4.7-fold). These effects of PRL were specific to the tuberoinfundibular DA neurons, as DA turnover was unaffected in nigrostriatal, mesolimbic, and incertohypothalamic DA neurons, and no changes were observed in NE turnover in any study area. The results support the involvement of PRL in the short loop feedback regulation of its own secretion in the MEm. The data further demonstrate a hypothalamic mechanism in the MEl by which hyperprolactinemia could inhibit LHRH release.

Animals↗
PubMedDate not supplied

Rapid release of substance P and LH-RH from synaptosomes prepared from the medial basal hypothalamus and substantia nigra.

We investigated Ca2+-dependent, depolarization-induced release of substance P (SP) and LH-RH from medial basal hypothalamic (MBH) and substantia nigra (SN) synaptosomes prepared from male rat brain. Depolarization of MBH synaptosomes evoked significant release of SP from 10.0 +/- 0.1 (5 mM K+) to 28.0 +/- 2.4 (75 mM K+) pg released/10 seconds. Fractional release was 1.0% and 2.7% respectively. In contrast, LH-RH was not released by depolarization of MBH synaptosomes: 11.6 +/- 0.9 (5 mM K+) to 11.0 +/- 0.7 (75 mM K+) pg released/10 seconds. Fractional release was 1.1 and 1.0% respectively. Depolarization-induced LH-RH release also did not occur in the presence of 10(-4) or 10(-6) M norepinephrine, 10(-7) M 12-O-tetradecanoylphorbol-13-acetate (TPA, PMA), 10(-5) M forskolin or in female rats. The inability of depolarizing concentrations of K+ to stimulate LH-RH release in physiological buffers remains an enigma. Significant depolarization-induced SP release was seen from MBH and SN synaptosomes at 20, 15, 10, 5 and only 1 second of release. Despite comparable basal release of SP from MBH and SN synaptosomes, the rate and magnitude of evoked release were much more pronounced in SN synaptosomes. The initial rate (0-1 second) of SP release was 4.5-fold greater from SN than from MBH synaptosomes [krel = 0.027(-1) (SN), krel = 0.006(-1) (MBH)]. The magnitude of SP release from SN synaptosomes was 2- to 3-fold greater at any given time interval compared with release from MBH synaptosomes.(ABSTRACT TRUNCATED AT 250 WORDS)

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